Emerging evidence supports the idea that adolescence is a unique developmental period during which time[unreadable] individuals are more likely to experiment with drugs of abuse and are at greater risk for subsequent[unreadable] addiction. There is a strong correlation between the onset of nicotine addiction at an early age and addiction[unreadable] to alcohol as well as a heightened vulnerability to addiction to either ethanol or nicotine when use is initiated[unreadable] during adolescence. When the brain is exposed to drugs of abuse, adaptive changes take place that[unreadable] contribute to the addictive process. Evidence demonstrates that many drugs alter the expression and activity[unreadable] of two major transcription factors, viz., cAMP response element binding protein (CREB) and deltaFosB (a[unreadable] truncated form of FosB) and that these alterations lead to the expression of genes thought to mediate the[unreadable] addictive process. Although studies have suggested that CREB and deltaFosB may represent a common[unreadable] cellular target for the action of addictive drugs, few studies have focused on the cellular consequences of[unreadable] exposure to nicotine and subsequent vulnerability to alcohol, targeting the two most widely used/abused and[unreadable] coabused compounds in the adolescent population.